Evidence map›Paper›PMID 21544581›Full record

ArticleHuman genetics2011

The X-inactivation trans-activator Rnf12 is negatively regulated by pluripotency factors in embryonic stem cells.

Pablo Navarro, Michael Moffat, Nicholas P Mullin, Ian Chambers

Open access · hybridAbstract read
In one paragraph

Article in Human genetics, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.

0numbers the graph read from it
0cells of the map it votes in
34citing papers in PubMed
5.2field-weighted citation impact, top 4% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

34 citing papers in PubMed, 54 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Article
  5. Cohesin controls X chromosome structure remodeling and X-reactivation during mouse iPSC-reprogramming.Proceedings of the National Academy of Sciences of the United States of America · 2023
    Article
  6. A long noncoding RNA influences the choice of the X chromosome to be inactivated.Proceedings of the National Academy of Sciences of the United States of America · 2022
    Article
  7. The Molecular and Nuclear Dynamics of X-Chromosome Inactivation.Cold Spring Harbor perspectives in biology · 2022
    Review
  8. A NovelMolecular and cellular biology · 2021
    Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Impaired imprinted X chromosome inactivation is responsible for the skewed sex ratio following in vitro fertilization.Proceedings of the National Academy of Sciences of the United States of America · 2016
    Article
  16. Review
  17. Review
  18. Article
  19. Article
  20. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

4 authors at 2 institutions in 1 country.

Pablo NavarroMRC Centre for Regenerative Medicine, Institute for Stem Cell Research, School of Biological Sciences, University of Edinburgh, King's Buildings, West Mains Road, Edinburgh EH9 3JQ, Scotland, UK. pablo.navarro@ed.ac.uk
Michael Moffat
Nicholas P Mullin
Ian Chambers
MRC Centre for Regenerative Medicine · GBUniversity of Edinburgh · GB

Funding

Wellcome Trust
6 · The paper itself

Abstract

X-inactivation, the molecular mechanism enabling dosage compensation in mammals, is tightly controlled during mouse early embryogenesis. In the morula, X-inactivation is imprinted with exclusive silencing of the paternally inherited X-chromosome. In contrast, in the post-implantation epiblast, X-inactivation affects randomly either the paternal or the maternal X-chromosome. The transition from imprinted to random X-inactivation takes place in the inner cell mass (ICM) of the blastocyst from which embryonic stem (ES) cells are derived. The trigger of X-inactivation, Xist, is specifically downregulated in the pluripotent cells of the ICM, thereby ensuring the reactivation of the inactive paternal X-chromosome and the transient presence of two active X-chromosomes. Moreover, Tsix, a critical cis-repressor of Xist, is upregulated in the ICM and in ES cells where it imposes a particular chromatin state at the Xist promoter that ensures the establishment of random X-inactivation upon differentiation. Recently, we have shown that key transcription factors supporting pluripotency directly repress Xist and activate Tsix and thus couple Xist/Tsix control to pluripotency. In this manuscript, we report that Rnf12, a third X-linked gene critical for the regulation of X-inactivation, is under the control of Nanog, Oct4 and Sox2, the three factors lying at the heart of the pluripotency network. We conclude that in mouse ES cells the pluripotency-associated machinery exerts an exhaustive control of X-inactivation by taking over the regulation of all three major regulators of X-inactivation: Xist, Tsix, and Rnf12.

Indexed as

AnimalsCell LineChromatin ImmunoprecipitationDNA PrimersEmbryonic Stem CellsGene Expression RegulationHomeodomain ProteinsMiceNanog Homeobox ProteinOctamer Transcription Factor-3Repressor ProteinsReverse Transcriptase Polymerase Chain ReactionRNA, Long NoncodingRNA, UntranslatedSOXB1 Transcription FactorsUbiquitin-Protein LigasesDNA PrimersHomeodomain ProteinsNanog Homeobox ProteinNanog protein, mouseOctamer Transcription Factor-3Pou5f1 protein, mouseRepressor ProteinsRlim protein, mouseRNA, Long NoncodingRNA, UntranslatedSox2 protein, mouseSOXB1 Transcription FactorsTsix transcript, mouseUbiquitin-Protein LigasesXIST non-coding RNA

Identifiers

PMID21544581
PMCPMC3132432
OpenAlexW2143567023

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.